Factors that directly affect axonal impulse conduction could also interact with other membrane channels. For example, potassium channels play an important role in setting the resting membrane potential of neurons. Enhancing the activity of specific potassium channels can prevent the depolarization of nerve membrane needed to initiate the generation of action potentials and impulse transmission. On the other hand, reducing the activity of specific potassium channels could lead to prolonged depolarization of nerves, which, as is discussed previously, can induce inacti-vation of voltage-gated sodium channels, leading to a depolarization block of impulse conduction. Fatty acids can increase the activity of potassium currents (Bendahhou and Agnew, 1996) as well as inhibiting sodium currents (Hong et al., 2004; Vreugdenhil et al., 1996) and could behave as neuroelectric blocking factors. Nitric oxide has also been reported to have affects on ion channels other than sodium channels. Nitric oxide activates large-conductance calcium-activated potassium (BK) channels in pituitary nerve terminals (Ahern et al., 1999). ATP-sensitive potassium (KATP) channels are also stimulated by nitric oxide (Lin et al., 2004). An increase of BK or KATP potassium current by nitric oxide is expected to suppress nerve excitability and therefore could also contribute to decreased impulse activity. Nitric oxide may also regulate neuronal activity by modulating calcium channels (Carabelli et al., 2002; D'Ascenzo et al., 2002). Reduction of calcium channel activity by nitric oxide would be expected to reduce neuronal excitability. However, although voltage-gated calcium channels may be expressed on astrocytes and oligodendrocytes in spinal cord white matter, they do not seem to be expressed on axons (Agrawal et al., 2000); therefore it is not clear what role inhibition of these channels might play in modulating axonal conduction.
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